We evaluated the therapeutic response by quantifying the percentage of cells expressing Ki67 (a proliferation marker) and CD44 (an invasion marker), showing that the downregulation of TMSB10 significantly improved the efficacy of PD1 inhibitors as well as selumetinib in GBM, and the combination of the three treatment strategies was the most effective (Fig. 8K). The gene discussed is TMSB10; the disease is glioblastoma.